scholarly journals Immunity to protozoan parasite infection (PP-002)

2010 ◽  
Vol 22 (Suppl_1_Pt_1) ◽  
pp. i23-i35
2001 ◽  
Vol 69 (9) ◽  
pp. 5940-5942 ◽  
Author(s):  
David A. Elliott ◽  
Daniel J. Coleman ◽  
Michael A. Lane ◽  
Robin C. May ◽  
Laura M. Machesky ◽  
...  

ABSTRACT The intracellular protozoan parasite Cryptosporidium parvum accumulates host cell actin at the interface between the parasite and the host cell cytoplasm. Here we show that the actin polymerizing proteins Arp2/3, vasodilator-stimulated phosphoprotein (VASP), and neural Wiskott Aldrich syndrome protein (N-WASP) are present at this interface and that host cell actin polymerization is necessary for parasite infection.


2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Melody Wickstrom ◽  
Madison Schanz ◽  
Kimberly Larson ◽  
Américo H. López-Yglesias

Background/Objective: The protozoan parasite Toxoplasma gondii is the second leading cause of foodborne pathogen-related deaths in the United States. The transcription factor T-bet is indispensable for host immunity against T. gondii. The absence of T-bet results in rapid susceptibility during parasite infection. T-bet has been considered essential for T-cell-derived IFN-g during T. gondii infection; yet, recent research has shown that T-bet is not required for lymphocyte-derived IFN-g responses. Our preliminary research shows that T-bet-deficient mice succumb to parasite infection significantly quicker than mice lacking lymphocytes. This has led to our hypothesis that T-bet-dependent myeloid cells are critical for host resistance during acute intestinal T. gondii infection. The objective of this project was to define the location of the T-bet-expressing myeloid cells in the medial small intestines (MSI) of naïve and infected mice during acute mucosal parasite infection. Methods: We used immunofluorescence microscopy to determine the location of T-bet-expressing myeloid cells in the MSI of naïve and T. gondii infected mice. Mice were orally infected with 40 cysts of the ME49 strain of T. gondii. On days 0 and 5, one-inch MSI segments were harvested, fixed with 4% paraformaldehyde for at least one hour, and then frozen in OCT compound. Tissues were then cut into 8mm sections and placed onto slides for staining. Sections were stained for nuclei, CD11c, T-bet, and T. gondii. Results: Our results revealed T-bet-expressing CD11c+ cells in both the MSI and spleen on days 0 and 5 of T. gondii infection. Summary: These data indicate that T-bet-expressing myeloid cells are present in the MSI during T. gondii infection. Defining the position of these cells will allow us to determine T-bet’s role in mediating myeloid cell-dependent T. gondii clearance. Due to the limited treatment options for patients suffering from toxoplasmosis it is critical to define new mechanisms for eliminating T. gondii.


The Nucleus ◽  
2021 ◽  
Author(s):  
Souradeepa Ghosh ◽  
Snehlata ◽  
Shahbaj Hussain ◽  
Himani Makkar ◽  
Budhaditya Mukherjee

PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e5046 ◽  
Author(s):  
Jennafer C. Malek ◽  
James E. Byers

Background Changes in climate are predicted to influence parasite and pathogen infection patterns in terrestrial and marine environments. Increases in temperature in particular may greatly alter biological processes, such as host-parasite interactions. For example, parasites could differentially benefit from increased reproduction and transmission or hosts could benefit from elevated immune responses that may mediate or even eliminate infections. In the southeastern United States, the Eastern oyster, Crassostrea virginica, is infected by the lethal protozoan parasite, Perkinsus marinus. Under field conditions, intertidal (air-exposed) oysters have been found to have significantly higher P. marinus infection intensity and marginally higher infection prevalence than subtidal (submerged) oysters. During summer, air temperatures are much warmer than water and this exposure of intertidal oysters to higher temperatures is a suggested mechanism for increased infection intensity. Methods We simulated intertidal exposure using controlled laboratory experiments to determine how host traits (survival and immune response) and parasite infection intensity will respond to elevated air temperature ranging from 27 °C to 53 °C during emersion at low tide. In Georgia, where our work was conducted, the average summer water temperature is 29 °C and the average maximum high air temperature in July is 33 °C (though oysters have been shown to survive at much higher air temperatures). Results Host survival declined as temperature increased, with a definitive drop-off between 39–43 °C. Negative effects of air temperature on host immune response (phagocytic activity) were detectable only at extremely high temperatures (47–50 °C) when hosts were suffering acute mortality. Parasite infection intensity peaked at 35 °C. Discussion Our results suggest that an increase in average summer air temperature to 35 °C or higher could affect oyster survival directly through temperature-related impacts in the short-term and indirectly through increased P. marinus infection intensity over the long-term.


2021 ◽  
Vol 12 ◽  
Author(s):  
Jing Zhang ◽  
Ying Sun ◽  
Jingtong Zheng

Protozoan parasite infection causes severe diseases in humans and animals, leading to tremendous economic and medical pressure. Natural immunity is the first line of defence against parasitic infection. Currently, the role of natural host immunity in combatting parasitic infection is unclear, so further research on natural host immunity against parasites will provide a theoretical basis for the prevention and treatment of related parasitic diseases. Extracellular traps (ETs) are an important natural mechanism of immunity involving resistance to pathogens. When immune cells such as neutrophils and macrophages are stimulated by external pathogens, they release a fibrous network structure, consisting mainly of DNA and protein, that can capture and kill a variety of extracellular pathogenic microorganisms. In this review, we discuss the relevant recently reported data on ET formation induced by protozoan parasite infection, including the molecular mechanisms involved, and discuss the role of ETs in the occurrence and development of parasitic diseases.


Author(s):  
Victor Tsutsumi ◽  
Adolfo Martinez-Palomo ◽  
Kyuichi Tanikawa

The protozoan parasite Entamoeba histolytica is the causative agent of amebiasis in man. The trophozoite or motile form is a highly dynamic and pleomorphic cell with a great capacity to destroy tissues. Moreover, the parasite has the singular ability to phagocytize a variety of different live or death cells. Phagocytosis of red blood cells by E. histolytica trophozoites is a complex phenomenon related with amebic pathogenicity and nutrition.


Planta Medica ◽  
2007 ◽  
Vol 73 (09) ◽  
Author(s):  
E Xingi ◽  
D Smirlis ◽  
S Bisti ◽  
V Myrianthopoulos ◽  
P Magiatis ◽  
...  

2017 ◽  
pp. 119-124
Author(s):  

Introduction: Intestinal parasite infections werecommonintropical country such as Vietnam. Having good knowledge of parasitic infectious prevention and changing risk behaviors can decrease the infection rate. Objective: To evaluate the parasitic infectious rate in Vinh Thai community before and after being health education and the changing of knowledge of parasitic infectious prevention and risk behaviors. Materials and methods: 60 households in Vinh Thai commune were interviewed their knowledge of parasitic infectious prevention and examined intestinal parasite infection by Kato technique and then trained the knowledge of parasitic infectious prevention. The interview and examination parasite infectiousrate were carried out after 6 months to evaluating their knowledge. Result: Before health education, the rate of intestinal parasite infection was 17.4% with the prevalence of Ascaris lumbricoides, hookworm, whipworm, pinworm, small fluke worm and co-infection with A. lumbricoides - whipworm, hookworm-whipworm were 0.1%; 8.0%; 5.8%; 0.6%; 0.3%; 1.2% and 3.0% respectively. Six months later the rate of intestinal parasite infection was decreased in 12.6% even though not statistical significantly. However, there were no case of small fluke worm and co-infection with hookworm-whipworm. Receiving health education, their knowledge of parasitic infectious prevention was higher significantly but their risk behaviors were not changed so much. Conclusion: Health education can change the rate of parasite infection with higher knowledge of parasitic infectious prevention but it was necessary continuous study to change the risk behaviors. Key words: intestinal parasite, health education


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